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Persistent infection with Listeria monocytogenes in the kidney induces anti‐inflammatory invariant fetal‐type γδ T cells
Author(s) -
Ikebe H.,
Yamada H.,
Nomoto M.,
Takimoto H.,
Nakamura T.,
Sonoda K.H.,
Nomoto K.
Publication year - 2001
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.2001.01149.x
Subject(s) - listeria monocytogenes , t cell receptor , t cell , biology , peritoneal cavity , immunology , inflammation , fetus , cd3 , antigen , immune system , cd8 , bacteria , anatomy , pregnancy , genetics
Summary After intraperitoneal inoculation with Listeria monocytogenes , γδ T cells appear in the peritoneal cavity preceding the appearance of αβ T cells. Such γδ T cells predominantly express T‐cell receptor (TCR)Vγ1/Vδ6, develop through an extrathymic pathway, and contribute to host defence against the bacteria. We have observed a gradual increase in γδ T cells in kidneys of mice after intrarenal inoculation with L. monocytogenes , which resulted in an unusually long‐lasting local infection. In this study, we examined the characteristics and the roles of the γδ T cells induced in this model. It was found that these γδ T cells predominantly expressed TCRVγ6/Vδ1 with canonical junctional sequences identical to those expressed on fetal thymocytes. Although depletion of such γδ T cells in vivo did not affect the number of bacteria, it resulted in histologically exacerbated inflammation in the kidneys. These results indicate that a persistent infection with L. monocytogenes in kidneys induces a different kind of γδ T cell from that induced after intraperitoneal infection. The former expresses invariant fetal‐type Vγ6/Vδ1 + TCR and plays a regulatory role in resolution of inflammation.